1. Registering for the Forum

    We require a human profile pic upon registration on this forum.

    After registration is submitted, you will receive a confirmation email, which should contain a link to confirm your intent to register for the forum. At this point, you will not yet be registered on the forum.

    Our Support staff will manually approve your account within 24 hours, and you will get a notification. This is to prevent the many spam account signups which we receive on a daily basis.

    If you have any problems completing this registration, please email support@jackkruse.com and we will assist you.

2017 science now firmly calls T2D a mitochondrial illness.

Discussion in 'Educating Doctors' started by Jack Kruse, Sep 28, 2017.

  1. Jack Kruse

    Jack Kruse Administrator

    Looks like 2017 science is finally realizing the foundational relationship of mitochondria to disease generation via heteroplasmy. This paper will be the first of many and is critical for all diabetics to read. Diabetes is a mitochondrial disease. This vindicates Dr. Wallace and myself for pounding the table on looking to mitochondria dysfunction as the cause of insulin resistance and diabetes.

    CITE: https://www.ncbi.nlm.nih.gov/pubmed/28951827

    How can we heal mitochondria that are destroyed by high heteroplasmy rates due to our poor environment? We need to optimize PGC-1 alpha signaling. How? Add electrons and lower protons to limit inflammation. Protons are another synonym for inflamation. protons = pH and pH that is low lowers the EZ in cell water. When the cell water EZ decreases light cannot make a battery in a cell. Paraoxonase serum concentration is influenced directly by pH changes and inflammatory changes and the levels of serum oxidized-LDL. Proliferator-activated receptor-γ (PPAR) has a co-activator called (PGC)-1 alpha. PGC-1 alpha is a member of a family of transcription co-activators that plays a central role in the regulation of all cellular energy metabolism. PGC-1 alpha protein may be also involved in controlling blood pressure, regulating cellular cholesterol homoeostasis, and the development of obesity and T2D. PGc-1 alpha also helps control mitochondrial number and density within a cell. Mitochondrial numbers are regulated by mitochondrial biogenesis to meet the energy demands of the cell and compensate for cell damage. This process is mediated by peroxisome proliferator–activated receptor γ coactivator 1α (PGC1α), which is relevant to mitochondrial dynamics since it is a transcriptional coactivator of the fusion mediator mitofusin-2. Mitofusin-2 is what connects the endoplasmic reticulum to mitochondria and control calcium homeostasis in the cell. Mitochondria– endoplasmic reticulum connectivity is regulated by mitofusin-2 and can create microdomains that facilitate fission.

    PGC-1 alpha can interact with, and regulate the activities of, cAMP response element binding protein (CREB) and nuclear respiratory factors (NRF’s) that allows us to make new mitochondria to produce more energy. CREB interacts with UV light as well in the brain to stimulate neuron growth. This is likely how exercise links to neocortical growth and repair in neuro-degeneration cases like Alzheimer’s disease. PGC-1 alpha is strongly induced by cold exposure. This is why I use ice when I exercise and swim in freezing water; it also links the environmental stimulus to adaptive thermogenesis (think UPC-1 from the leptin series). If one can mix this cold exposure to AM sunlight you really are doing yourself a big help in reversing diseases. The link to cold exposure and UV sunlight on the skin and circulatory system also involves AMPk pathways. The reason for this is how the AMP-activated protein kinase pathway (AMPk) works to these environment stimuli. The AMPk pathway is best described as a fuel sensor for lipid and glucose metabolism. Activated AMPk inhibits PPAR-{alpha} and PPAR-gamma . Cold exposure on our skin surfaces and face increase fat release from adipocytes. AMPk rises with cold. Ultraviolet radiation and reactive oxygen species from cytochrome 1 (ROS) impair the AMPk signaling axis. This is how AMPk works within a circadian cycle with UV light. Both leptin (nutrition success) and adiponectin (nutrition deprivation) activate AMPk pathways. Cold and UV light are at opposite ends of the circadian cycles but both work in unison to help us absorb UV light and assimilate it and transform it to a DC electric current to regenerate mitochondria. Metformin mimics cold exposure but it does not work ideally in a artificial lit environment.

    CITE: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3883043/
  2. Josh Rosenthal

    Josh Rosenthal Charter member of Purple Angels Club

    look at where it's published... falling on deaf ears... but GOOD news nonetheless.
  3. Jack Kruse

    Jack Kruse Administrator

    Richelle Jones likes this.

Share This Page